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Institute
Background
The anterior cruciate ligament (ACL) rupture can lead to impaired knee function. Reconstruction decreases the mechanical instability but might not have an impact on sensorimotor alterations.
Objective
Evaluation of the sensorimotor function measured with the active joint position sense (JPS) test in anterior cruciate ligament (ACL) reconstructed patients compared to the contralateral side and a healthy control group.
Methods
The databases MEDLINE, CINAHL, EMBASE, PEDro, Cochrane Library and SPORTDiscus were systematically searched from origin until April 2020. Studies published in English, German, French, Spanish or Italian language were included. Evaluation of the sensorimotor performance was restricted to the active joint position sense test in ACL reconstructed participants or healthy controls. The Preferred Items for Systematic Reviews and Meta-Analyses guidelines were followed. Study quality was evaluated using the Quality Assessment Tool for Observational Cohort and Cross-Sectional Studies. Data was descriptively synthesized.
Results
Ten studies were included after application of the selective criteria. Higher angular deviation, reaching significant difference (p < 0.001) in one study, was shown up to three months after surgery in the affected limb. Six months post-operative significantly less error (p < 0.01) was found in the reconstructed leg compared to the contralateral side and healthy controls. One or more years after ACL reconstruction significant differences were inconsistent along the studies.
Conclusions
Altered sensorimotor function was present after ACL reconstruction. Due to inconsistencies and small magnitudes, clinical relevance might be questionable. JPS testing can be performed in acute injured persons and prospective studies could enhance knowledge of sensorimotor function throughout the rehabilitative processes.
Background
The anterior cruciate ligament (ACL) rupture can lead to impaired knee function. Reconstruction decreases the mechanical instability but might not have an impact on sensorimotor alterations.
Objective
Evaluation of the sensorimotor function measured with the active joint position sense (JPS) test in anterior cruciate ligament (ACL) reconstructed patients compared to the contralateral side and a healthy control group.
Methods
The databases MEDLINE, CINAHL, EMBASE, PEDro, Cochrane Library and SPORTDiscus were systematically searched from origin until April 2020. Studies published in English, German, French, Spanish or Italian language were included. Evaluation of the sensorimotor performance was restricted to the active joint position sense test in ACL reconstructed participants or healthy controls. The Preferred Items for Systematic Reviews and Meta-Analyses guidelines were followed. Study quality was evaluated using the Quality Assessment Tool for Observational Cohort and Cross-Sectional Studies. Data was descriptively synthesized.
Results
Ten studies were included after application of the selective criteria. Higher angular deviation, reaching significant difference (p < 0.001) in one study, was shown up to three months after surgery in the affected limb. Six months post-operative significantly less error (p < 0.01) was found in the reconstructed leg compared to the contralateral side and healthy controls. One or more years after ACL reconstruction significant differences were inconsistent along the studies.
Conclusions
Altered sensorimotor function was present after ACL reconstruction. Due to inconsistencies and small magnitudes, clinical relevance might be questionable. JPS testing can be performed in acute injured persons and prospective studies could enhance knowledge of sensorimotor function throughout the rehabilitative processes.
Eccentric exercise is discussed as a treatment option for clinical populations, but specific responses in terms of muscle damage and systemic inflammation after repeated loading of large muscle groups have not been conclusively characterized. Therefore, this study tested the feasibility of an isokinetic protocol for repeated maximum eccentric loading of the trunk muscles. Nine asymptomatic participants (5 f/4 m; 34±6 yrs; 175±13 cm; 76±17 kg) performed three isokinetic 2-minute all-out trunk strength tests (1x concentric (CON), 2x eccentric (ECC1, ECC2), 2 weeks apart; flexion/extension, 60°/s, ROM 55°). Outcomes were peak torque, torque decline, total work, and indicators of muscle damage and inflammation (over 168 h). Statistics were done using the Friedman test (Dunn’s post-test). For ECC1 and ECC2, peak torque and total work were increased and torque decline reduced compared to CON. Repeated ECC bouts yielded unaltered torque and work outcomes. Muscle damage markers were highest after ECC1 (soreness 48 h, creatine kinase 72 h; p<0.05). Their overall responses (area under the curve) were abolished post-ECC2 compared to post-ECC1 (p<0.05). Interleukin-6 was higher post-ECC1 than CON, and attenuated post-ECC2 (p>0.05). Interleukin-10 and tumor necrosis factor-α were not detectable. All markers showed high inter-individual variability. The protocol was feasible to induce muscle damage indicators after exercising a large muscle group, but the pilot results indicated only weak systemic inflammatory responses in asymptomatic adults.
Eccentric exercise is discussed as a treatment option for clinical populations, but specific responses in terms of muscle damage and systemic inflammation after repeated loading of large muscle groups have not been conclusively characterized. Therefore, this study tested the feasibility of an isokinetic protocol for repeated maximum eccentric loading of the trunk muscles. Nine asymptomatic participants (5 f/4 m; 34±6 yrs; 175±13 cm; 76±17 kg) performed three isokinetic 2-minute all-out trunk strength tests (1x concentric (CON), 2x eccentric (ECC1, ECC2), 2 weeks apart; flexion/extension, 60°/s, ROM 55°). Outcomes were peak torque, torque decline, total work, and indicators of muscle damage and inflammation (over 168 h). Statistics were done using the Friedman test (Dunn’s post-test). For ECC1 and ECC2, peak torque and total work were increased and torque decline reduced compared to CON. Repeated ECC bouts yielded unaltered torque and work outcomes. Muscle damage markers were highest after ECC1 (soreness 48 h, creatine kinase 72 h; p<0.05). Their overall responses (area under the curve) were abolished post-ECC2 compared to post-ECC1 (p<0.05). Interleukin-6 was higher post-ECC1 than CON, and attenuated post-ECC2 (p>0.05). Interleukin-10 and tumor necrosis factor-α were not detectable. All markers showed high inter-individual variability. The protocol was feasible to induce muscle damage indicators after exercising a large muscle group, but the pilot results indicated only weak systemic inflammatory responses in asymptomatic adults.
Background Recent studies indicate the existence of a repeated bout effect on the contralateral untrained limb following eccentric and isometric contractions. Aims This review aims to summarize the evidence for magnitude, duration and differences of this effect following isometric and eccentric preconditioning exercises. Methods Medline, Cochrane, and Web of science were searched from January 1971 until September 2020. Randomized controlled trials, case-control studies and cross-sectional studies were identified by combining keywords and synonyms (e.g., "contralateral", "exercise", "preconditioning", "protective effect"). At least two of the following outcome parameters were mandatory for study inclusion: strength, muscle soreness, muscle swelling, limb circumference, inflammatory blood markers or protective index (relative change of aforementioned measures). Results After identifying 1979 articles, 13 studies were included. Most investigations examined elbow flexors and utilized eccentric isokinetic protocols to induce the contralateral repeated bout effect. The magnitude of protection was observed in four studies, smaller values of the contralateral when compared to the ipsilateral repeated bout effect were noted in three studies. The potential mechanism is thought to be of neural central nature since no differences in peripheral muscle activity were observed. Time course was examined in three investigations. One study showed a smaller protective effect following isometric preconditioning when compared to eccentric preconditioning exercises. Conclusions The contralateral repeated bout effect demonstrates a smaller magnitude and lasts shorter than the ipsilateral repeated bout effect. Future research should incorporate long-term controlled trials including larger populations to identify central mechanisms. This knowledge should be used in clinical practice to prepare immobilized limbs prospectively for an incremental load.
Background: Chronic ankle instability, developing from ankle sprain, is one of the most common sports injuries. Besides it being an ankle issue, chronic ankle instability can also cause additional injuries. Investigating the epidemiology of chronic ankle instability is an essential step to develop an adequate injury prevention strategy. However, the epidemiology of chronic ankle instability remains unknown. Therefore, the purpose of this study was to investigate the epidemiology of chronic ankle instability through valid and reliable self-reported tools in active populations.
Methods: An electronic search was performed on PubMed and Web of Science in July 2020. The inclusion criteria for articles were peer-reviewed, published between 2006 and 2020, using one of the valid and reliable tools to evaluate ankle instability, determining chronic ankle instability based on the criteria of the International Ankle
Consortium, and including the outcome of epidemiology of chronic ankle instability. The risk of bias of the included studies was evaluated with an adapted tool for the sports injury review method.
Results: After removing duplicated studies, 593 articles were screened for eligibility. Twenty full-texts were screened and finally nine studies were included, assessing 3804 participants in total. The participants were between 15 and 32 years old and represented soldiers, students, athletes and active individuals with a history of ankle sprain. The prevalence of chronic ankle instability was 25%, ranging between 7 and 53%. The prevalence of chronic ankle instability within participants with a history of ankle sprains was 46%, ranging between 9 and 76%. Five included studies identified chronic ankle instability based on the standard criteria, and four studies applied adapted exclusion criteria to conduct the study. Five out of nine included studies showed a low risk of bias.
Conclusions: The prevalence of chronic ankle instability shows a wide range. This could be due to the different exclusion criteria, age, sports discipline, or other factors among the included studies. For future studies, standardized criteria to investigate the epidemiology of chronic ankle instability are required. The epidemiology of
CAI should be prospective. Factors affecting the prevalence of chronic ankle instability should be investigated and clearly described.
Background: Chronic ankle instability, developing from ankle sprain, is one of the most common sports injuries. Besides it being an ankle issue, chronic ankle instability can also cause additional injuries. Investigating the epidemiology of chronic ankle instability is an essential step to develop an adequate injury prevention strategy. However, the epidemiology of chronic ankle instability remains unknown. Therefore, the purpose of this study was to investigate the epidemiology of chronic ankle instability through valid and reliable self-reported tools in active populations.
Methods: An electronic search was performed on PubMed and Web of Science in July 2020. The inclusion criteria for articles were peer-reviewed, published between 2006 and 2020, using one of the valid and reliable tools to evaluate ankle instability, determining chronic ankle instability based on the criteria of the International Ankle
Consortium, and including the outcome of epidemiology of chronic ankle instability. The risk of bias of the included studies was evaluated with an adapted tool for the sports injury review method.
Results: After removing duplicated studies, 593 articles were screened for eligibility. Twenty full-texts were screened and finally nine studies were included, assessing 3804 participants in total. The participants were between 15 and 32 years old and represented soldiers, students, athletes and active individuals with a history of ankle sprain. The prevalence of chronic ankle instability was 25%, ranging between 7 and 53%. The prevalence of chronic ankle instability within participants with a history of ankle sprains was 46%, ranging between 9 and 76%. Five included studies identified chronic ankle instability based on the standard criteria, and four studies applied adapted exclusion criteria to conduct the study. Five out of nine included studies showed a low risk of bias.
Conclusions: The prevalence of chronic ankle instability shows a wide range. This could be due to the different exclusion criteria, age, sports discipline, or other factors among the included studies. For future studies, standardized criteria to investigate the epidemiology of chronic ankle instability are required. The epidemiology of
CAI should be prospective. Factors affecting the prevalence of chronic ankle instability should be investigated and clearly described.
Background/Purpose
Muscular reflex responses of the lower extremities to sudden gait disturbances are related to postural stability and injury risk. Chronic ankle instability (CAI) has shown to affect activities related to the distal leg muscles while walking. Its effects on proximal muscle activities of the leg, both for the injured- (IN) and uninjured-side (NON), remain unclear. Therefore, the aim was to compare the difference of the motor control strategy in ipsilateral and contralateral proximal joints while unperturbed walking and perturbed walking between individuals with CAI and matched controls.
Materials and methods
In a cross-sectional study, 13 participants with unilateral CAI and 13 controls (CON) walked on a split-belt treadmill with and without random left- and right-sided perturbations. EMG amplitudes of muscles at lower extremities were analyzed 200 ms after perturbations, 200 ms before, and 100 ms after (Post100) heel contact while walking. Onset latencies were analyzed at heel contacts and after perturbations. Statistical significance was set at alpha≤0.05 and 95% confidence intervals were applied to determine group differences. Cohen’s d effect sizes were calculated to evaluate the extent of differences.
Results
Participants with CAI showed increased EMG amplitudes for NON-rectus abdominus at Post100 and shorter latencies for IN-gluteus maximus after heel contact compared to CON (p<0.05). Overall, leg muscles (rectus femoris, biceps femoris, and gluteus medius) activated earlier and less bilaterally (d = 0.30–0.88) and trunk muscles (bilateral rectus abdominus and NON-erector spinae) activated earlier and more for the CAI group than CON group (d = 0.33–1.09).
Conclusion
Unilateral CAI alters the pattern of the motor control strategy around proximal joints bilaterally. Neuromuscular training for the muscles, which alters motor control strategy because of CAI, could be taken into consideration when planning rehabilitation for CAI.
Background: The relationship between exercise-induced intratendinous blood flow (IBF) and tendon pathology or training exposure is unclear.
Objective: This study investigates the acute effect of running exercise on sonographic detectable IBF in healthy and tendinopathic Achilles tendons (ATs) of runners and recreational participants.
Methods: 48 participants (43 ± 13 years, 176 ± 9 cm, 75 ± 11 kg) performed a standardized submaximal 30-min constant load treadmill run with Doppler ultrasound “Advanced dynamic flow” examinations before (Upre) and 5, 30, 60, and 120 min (U5-U120) afterward. Included were runners (>30 km/week) and recreational participants (<10 km/week) with healthy (Hrun, n = 10; Hrec, n = 15) or tendinopathic (Trun, n = 13; Trec, n = 10) ATs. IBF was assessed by counting number [n] of intratendinous vessels. IBF data are presented descriptively (%, median [minimum to maximum range] for baseline-IBF and IBF-difference post-exercise). Statistical differences for group and time point IBF and IBF changes were analyzed with Friedman and Kruskal-Wallis ANOVA (α = 0.05).
Results: At baseline, IBF was detected in 40% (3 [1–6]) of Hrun, in 53% (4 [1–5]) of Hrec, in 85% (3 [1–25]) of Trun, and 70% (10 [2–30]) of Trec. At U5 IBF responded to exercise in 30% (3 [−1–9]) of Hrun, in 53% (4 [−2–6]) of Hrec, in 70% (4 [−10–10]) of Trun, and in 80% (5 [1–10]) of Trec. While IBF in 80% of healthy responding ATs returned to baseline at U30, IBF remained elevated until U120 in 60% of tendinopathic ATs. Within groups, IBF changes from Upre-U120 were significant for Hrec (p < 0.01), Trun (p = 0.05), and Trec (p < 0.01). Between groups, IBF changes in consecutive examinations were not significantly different (p > 0.05) but IBF-level was significantly higher at all measurement time points in tendinopathic versus healthy ATs (p < 0.05).
Conclusion: Irrespective of training status and tendon pathology, running leads to an immediate increase of IBF in responding tendons. This increase occurs shortly in healthy and prolonged in tendinopathic ATs. Training exposure does not alter IBF occurrence, but IBF level is elevated in tendon pathology. While an immediate exercise-induced IBF increase is a physiological response, prolonged IBF is considered a pathological finding associated with Achilles tendinopathy.
Background: The relationship between exercise-induced intratendinous blood flow (IBF) and tendon pathology or training exposure is unclear.
Objective: This study investigates the acute effect of running exercise on sonographic detectable IBF in healthy and tendinopathic Achilles tendons (ATs) of runners and recreational participants.
Methods: 48 participants (43 ± 13 years, 176 ± 9 cm, 75 ± 11 kg) performed a standardized submaximal 30-min constant load treadmill run with Doppler ultrasound “Advanced dynamic flow” examinations before (Upre) and 5, 30, 60, and 120 min (U5-U120) afterward. Included were runners (>30 km/week) and recreational participants (<10 km/week) with healthy (Hrun, n = 10; Hrec, n = 15) or tendinopathic (Trun, n = 13; Trec, n = 10) ATs. IBF was assessed by counting number [n] of intratendinous vessels. IBF data are presented descriptively (%, median [minimum to maximum range] for baseline-IBF and IBF-difference post-exercise). Statistical differences for group and time point IBF and IBF changes were analyzed with Friedman and Kruskal-Wallis ANOVA (α = 0.05).
Results: At baseline, IBF was detected in 40% (3 [1–6]) of Hrun, in 53% (4 [1–5]) of Hrec, in 85% (3 [1–25]) of Trun, and 70% (10 [2–30]) of Trec. At U5 IBF responded to exercise in 30% (3 [−1–9]) of Hrun, in 53% (4 [−2–6]) of Hrec, in 70% (4 [−10–10]) of Trun, and in 80% (5 [1–10]) of Trec. While IBF in 80% of healthy responding ATs returned to baseline at U30, IBF remained elevated until U120 in 60% of tendinopathic ATs. Within groups, IBF changes from Upre-U120 were significant for Hrec (p < 0.01), Trun (p = 0.05), and Trec (p < 0.01). Between groups, IBF changes in consecutive examinations were not significantly different (p > 0.05) but IBF-level was significantly higher at all measurement time points in tendinopathic versus healthy ATs (p < 0.05).
Conclusion: Irrespective of training status and tendon pathology, running leads to an immediate increase of IBF in responding tendons. This increase occurs shortly in healthy and prolonged in tendinopathic ATs. Training exposure does not alter IBF occurrence, but IBF level is elevated in tendon pathology. While an immediate exercise-induced IBF increase is a physiological response, prolonged IBF is considered a pathological finding associated with Achilles tendinopathy.